Loeb J M, Murdock D K, Randall W C, Euler D E
Circ Res. 1979 Mar;44(3):329-34. doi: 10.1161/01.res.44.3.329.
The ability to reduce and maintain heart rate by electrical stimulation (underdrive) was tested in three groups of chronically instrumented dogs: sinoatrial node intact, ectopic atrial pacemaker produced by injection of rapidly hardening latex into the sinoatrial nodal artery, and idioventricular pacemaker produced by injection of formalin into the atrioventricular node. In the conscious unsedated state, underdrive of sinoatrial or idioventricular pacemakers resulted in competition between driven and intrinsic foci. However, the cycle length of ectopic atrial pacemakers could be increased by 148.4 +/- 30.7 msec (P less than 0.001) and maintained at that value. Cessation of underdrive resulted in a period of pacemaker suppression similar to that produced following overdrive. Single premature stimuli produced marked cycle length prolongations in dogs with ectopic atrial foci. Total autonomic blockade had no significant effect on the production of underdrive. Thus, the results of the present experiments provide evidence for maintained capture of cardiac pacemakers at rates significantly below intrinsic control and indicate that underdrive varies as a function of pacemaker site. Underdrive may explain the failure of junctional escape in the presence of slower atrial rhythms.
在三组长期植入仪器的犬中测试了通过电刺激(超速抑制)降低并维持心率的能力:窦房结完整组、通过向窦房结动脉注射快速硬化乳胶产生异位心房起搏器组以及通过向房室结注射福尔马林产生心室自主节律起搏器组。在清醒未镇静状态下,对窦房结或心室自主节律起搏器进行超速抑制会导致驱动灶与固有起搏点之间的竞争。然而,异位心房起搏器的周期长度可增加148.4±30.7毫秒(P<0.001)并维持在该值。超速抑制停止会导致一段类似于超速驱动后产生的起搏器抑制期。单个过早刺激在有异位心房起搏点的犬中产生明显的周期长度延长。完全自主神经阻滞对超速抑制的产生无显著影响。因此,本实验结果为以显著低于固有控制的速率维持心脏起搏器的夺获提供了证据,并表明超速抑制随起搏点部位而变化。超速抑制可能解释了在心房节律较慢时交界性逸搏失败的原因。